mTOR contributes to endothelium-dependent vasorelaxation by promoting eNOS expression and preventing eNOS uncoupling

Abstract

The endothelium-specific inhibition of either of mammalian target of rapamycin (mTOR) complexes impairs endothelial-dependent vasodilatation (EDD), accompanied by decreased nitric oxide bioavailability in both human and mice endothelial cells.